Heterochromatinization associated with cell differentiation as a model to study DNA double strand break induction and repair in the context of higher-order chromatin structure
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
23454236
DOI
10.1016/j.apradiso.2013.01.029
PII: S0969-8043(13)00038-9
Knihovny.cz E-resources
- Keywords
- Chromatin sensitivity to DSB induction, DNA double strand break (DSB) repair, Heterochromatin, Higher-order chromatin structure, Immature and terminally differentiated granulocytes, γH2AX/53BP1 repair foci,
- MeSH
- Cell Differentiation * MeSH
- Chromatin chemistry MeSH
- In Situ Hybridization, Fluorescence MeSH
- Protein Conformation MeSH
- Cells, Cultured MeSH
- Humans MeSH
- DNA Repair * MeSH
- DNA Damage * MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Chromatin MeSH
Cell differentiation is associated with extensive gene silencing, heterochromatinization and potentially decreasing need for repairing DNA double-strand breaks (DSBs). Differentiation stages of blood cells thus represent an excellent model to study DSB induction, repair and misrepair in the context of changing higher-order chromatin structure. We show that immature granulocytes form γH2AX and 53BP1 foci, contrary to the mature cells; however, these foci colocalize only rarely and DSB repair is inefficient. Moreover, specific chromatin structure of granulocytes probably influences DSB induction.
References provided by Crossref.org
Spatial-Temporal Genome Regulation in Stress-Response and Cell-Fate Change
